Botulinum Toxin as a Pain Killer: Players and Actions in Antinociception

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초록

Botulinum neurotoxins (BoNTs) have been widely used to treat a variety of clinical ailments associated with pain. The inhibitory action of BoNTs on synaptic vesicle fusion blocks the releases of various pain-modulating neurotransmitters, including glutamate, substance P (SP), and calcitonin gene-related peptide (CGRP), as well as the addition of pain-sensing transmembrane receptors such as transient receptor potential (TRP) to neuronal plasma membrane. In addition, growing evidence suggests that the analgesic and anti-inflammatory effects of BoNTs are mediated through various molecular pathways. Recent studies have revealed that the detailed structural bases of BoNTs interact with their cellular receptors and SNAREs. In this review, we discuss the molecular and cellular mechanisms related to the efficacy of BoNTs in alleviating human pain and insights on engineering the toxins to extend therapeutic interventions related to nociception.

키워드

botulinum neurotoxinpainnociceptionneurotransmitterneuropeptideTRPNEUROTOXIN TYPE-ACLOSTRIDIUM-BOTULINUMLIGHT-CHAINCRYSTAL-STRUCTURESENSORY NEURONSEPITHELIAL BARRIERVANILLOID RECEPTORTRPV1 EXPRESSIONNERVE-TERMINALSPEPTIDE RELEASE
제목
Botulinum Toxin as a Pain Killer: Players and Actions in Antinociception
저자
Kim, Dong-WanLee, Sun-KyungAhnn, Joohong
DOI
10.3390/toxins7072435
발행일
2015-07
유형
Review
저널명
Toxins
7
7
페이지
2435 ~ 2453

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